Acute gastrointestinal bleeding

Chapter 36 Acute gastrointestinal bleeding



Joseph J Y. Sung


Acute gastrointestinal (GI) bleeding is a common admission to the intensive care unit (ICU) and a major cause of morbidity and mortality. Peptic ulcer disease accounts for 75% of upper GI bleeding.1,2 Bleeding from varices, oesophagitis, duodenitis and Mallory–Weiss syndrome each account for between 5% and 15% of cases. About 20% of GI bleeding arises from the lower GI tract. Common aetiological causes for GI bleeding are listed in Table 36.1. Mortality from upper GI bleeding has remained at approximately 10% for decades, but recent reports suggest that mortality from bleeding ulcers has fallen substantially to about 5%.3 On the other hand, variceal bleeding has a much higher mortality of about 30%. Risk factors for mortality include old age, associated medical problems, coagulopathy and magnitude of bleeding.


Table 36.1 Common causes of acute gastrointestinal bleeding



























Upper gastrointestinal bleeding
Peptic ulcers (DU:GU 3:1)
Varices (oesophageal varices:gastric varices 9:1)
Portal hypertensive gastropathy
Mallory–Weiss syndrome
Gastritis, duodenitis and oesophagitis
Lower gastrointestinal bleeding
Diverticular bleeding
Angiodysplasia and arteriovenous malformation
Colonic polyps or tumours
Meckel’s diverticulum
Inammatory bowel diseases

DU, duodenal ulcer; GU, gastrointestinal ulcer.



UPPER GASTROINTESTINAL BLEEDING



CLINICAL PRESENTATION


The patient may or may not present with a history of upper GI problems. There may be pain but bleeding ulcers can be painless, especially in elderly patients and users of non-steroidal anti-inflammatory drugs. Frequently, the symptoms of hypovolaemia such as tachycardia, pallor, sweating, cyanosis, mental confusion and oliguria may be present, especially in massive GI bleeding. A history of vomiting and retching preceding haematemesis suggests Mallory–Weiss syndrome.


Haematemesis and melaena are the most common presentations of acute upper GI bleeding. Haematochezia is the passage of bright red or maroon blood from the rectum, in the form of pure blood or admixed with stool. It usually represents a lower intestinal source of bleeding, but can also be a feature of massive upper GI bleeding.



INVESTIGATION



ENDOSCOPY OR BARIUM STUDY


As history and physical examination are seldom useful in identifying the source of bleeding, investigations are necessary in most cases of GI bleeding. Endoscopy has replaced barium studies as the investigation of choice. It should be performed as soon as the patient is haemodynamically stabilised, and adequate supportive personnel are available. Endoscopy is preferred to barium X-rays for the following reasons:


• Endoscopy allows more precise identification of the site and nature of bleeding.

• Endoscopic appearance often predicts the risk of recurrent bleeding from ulcer and varices (see below).

• Lesions such as gastritis, portal hypertensive gastropathy and duodenitis are difficult to diagnose by barium X-ray.

• Treatments such as injecting ulcers may be instigated during endoscopy (see below).

• Barium X-ray is notoriously unreliable in patients with previous gastric surgery.

However, endoscopy can induce serious hypoxia in patients with cardiorespiratory diseases. Continuous monitoring of blood pressure, pulse and oxygen saturation with a pulse oximeter is mandatory. Oxygen should be administered by nasal cannula when necessary.



ANGIOGRAPHY


Angiography is seldom used for the diagnosis of upper GI bleeding. Theoretically, when the bleeding is very brisk and obscures the endoscopic view, angiography may help to identify the sources of bleeding and may sometimes be used to embolise the bleeding point. In practice, however, most patients with this degree of haemorrhage should be considered for emergency laparotomy.



MANAGEMENT OF NON-VARICEAL UPPER GI BLEEDING


The goals of managing a patient with acute GI bleeding are first, to resuscitate; second, to control active bleeding; and third, to prevent recurrence of haemorrhage.



RESUSCITATION


Blood and plasma expanders should be given through large-bore intravenous cannulae. Vital signs should be closely monitored. In patients with hypovolaemic shock, central venous pressure and hourly urine output should also be observed (see Chapter 11). Following adequate resuscitation, management is directed to identify the lesion and distinguish the high-risk patient, who is likely to require early endoscopic or surgical treatment.



THE HIGH-RISK PATIENT


Significant GI bleeding is indicated by syncope, haematemesis, systolic blood pressure below 100 mmHg (13.3 kPa), postural hypotension and, if more than 4 units of blood have to be transfused in 12 hours, to maintain blood pressure. Patients over 60 years old and with multiple underlying diseases are at even higher risk.3 Those admitted for other medical problems (e.g. heart or respiratory failure, or cerebrovascular bleed) and who have GI bleeding during hospitalisation also have a higher mortality.



THE HIGH-RISK ULCER


Peptic ulcers that are actively bleeding or have bled recently may show stigmata of haemorrhage on endoscopy. These include localised active bleeding (i.e. pulsatile, arterial spurting or simple oozing), an adherent blood clot, a protuberant vessel or a flat pigmented spot on the ulcer base. Stigmata of haemorrhage are important predictors of recurrent bleeding (Table 36.2). The proximal postero inferior wall of the duodenal bulb and the high lesser curve of the stomach are common sites for severe recurrent bleeding, due probably to their respective large arteries (gastroduodenal and left gastric arteries).


Table 36.2 Stigmata of haemorrhage and risk of recurrent bleeding in peptic ulcers





















Stigmata of haemorrhage % recurrent bleeding
Spurter or oozer 85–90
Protuberant vessel 35–55
Adherent clot 30–40
Flat spot 5–10
None 5


TREATMENT



Pharmacological control


Acid-suppressing drugs such as H2-receptor antagonists and proton pump inhibitors are very effective drugs to promote ulcer healing. An acidic environment impairs platelet function and haemostasis. Therefore, reducing the secretion of gastric acid should reduce bleeding and encourage ulcer healing. A recent study has shown that potent acid suppression using intravenous proton pump inhibitors reduces recurrent bleeding after endoscopic therapy.4 Proton pump inhibitors should be recommended in high-risk peptic ulcer bleeding patients as an adjuvant to endoscopic therapy. In contrast, antifibrinolytic agents such as tranexamic acid have not been effective in reducing the operative rate and mortality of acute GI haemorrhage. Recent studies show that in patients at high risk of recurrent bleeding, pharmacologic control without endoscopic hemostasis is inadequate.5 Thus a combination of endoscopic and pharmacologic therapy offers the best therapy for ulcer bleeding patients.6,7



Endoscopic therapy


Most patients with acute upper GI haemorrhage stop bleeding spontaneously and have an uneventful recovery. No specific intervention is required in these patients. Endoscopic haemostasis should be used in patients with a high risk of persistent or recurrent bleeding. In the last two decades, endoscopic haemostasis, with its high efficacy and low morbidity, has resulted in a dramatic decrease in emergency surgery, and has reduced the mortality of ulcer bleeding. The three most popular methods of haemostasis are as follows.



Adrenaline (epinephrine) injection

Endoscopic injection of adrenaline (1:10 000 dilution) at 0.5–1.0-ml aliquots (up to 10–15 ml) into and around the ulcer bleeding point has achieved successful haemostasis in over 90% of cases.6 Debate exists as to whether the haemostatic effect is a result of local tamponade by the volume injected, or vasoconstriction by adrenaline. Absorption of adrenaline into the systemic circulation has been documented, but without any significant effect on the haemodynamic status of the patient.8 Adrenaline injection is an effective, cheap, portable and easy-to-learn method of haemostasis, and has acquired worldwide popularity.



Coaptive coagulation

This method uses direct pressure and heat energy (heater probe) or electrocoagulation (bipolar coagulation probe (BICAP)) to control ulcer bleeding. The depth of tissue injury induced by these devices is minimised, as the bleeding vessel is tamponaded prior to coagulation. The overall efficacy of the adrenaline injection, heater probe and BICAP probe methods is comparable.9 Occasionally, it is not possible to obtain a view en face of the bleeding ulcers, particularly those on the lesser curve or on the posterior wall of the duodenal bulb. In these situations, direct pressure cannot be applied, and the failure rate of coaptive coagulation in these situations is expected to be higher.



Haemoclips

Endoscopic clipping of a bleeding vessel is an appealing alternative treatment which has gained popularity in recent years. The advantage of haemoclips over thermocoagulation is that there is no tissue injury induced and hence the risk of perforation is reduced. Studies comparing haemoclips against injection and thermocoagulation have shown favourable results.10,11 However, the application of haemoclips in certain sites, for example lesser curve, gastric fundus and posterior wall of the duodenum, is technically difficult. Loading of clips on to the application device is cumbersome and time-consuming and transfer of torque from the handle to the tip of the device is limited.



SURGERY


Surgery remains the most definitive method of stopping haemorrhage. However, there is little agreement on the exact indications and best timing for surgical intervention. These issues are even less clear now that endoscopic treatment is so effective. Accordingly, good cooperation among intensivists, gastroenterologists and surgeons is essential. Indications for surgery can be:


• arterial bleeding that cannot be controlled by endoscopic haemostasis

• massive transfusion (i.e. total of 6–8 units of blood) required to maintain blood pressure

• recurrent clinical bleeding after initial success in endoscopic hemostasis

• evidence suggestive of GI perforation

Surgical procedures include underrunning of the ulcer, underrunning plus vagotomy and drainage, and various types of gastrectomy. The overall mortality of emergency surgery for GI bleeding is about 15–20%. In a study investigating the best salvage treatment for patients with recurrent bleeding after endoscopic therapy, surgery was found to be comparable to repeating endoscopic treatment in securing hemostasis.12 However, morbidity is significantly higher in surgical patients than in endoscopic patients. Early surgery should be considered in patients with hypovolaemic shock and/or large peptic ulcer with protuberant vessels. A protocol to manage bleeding peptic ulcer is shown in Figure 36.1.13


image

Figure 36.1 Management of peptic ulcer bleeding.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Acute gastrointestinal bleeding

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